Genetically cardiomyopathic Syrian hamster strains provide a unique animal model to reproducibly analyze the events which occur at predictable times and lead to the death of each hamster from heart failure. We propose to study heart structure and function in embryonic, neo- and post-natal cardiomyopathic (UM-X 7.1) (CM) and age-matched normal (N) hamsters. Our aim is to differentiate between conflicting results, from our laboratory and from others, on the early morphological development of CM heart--whether such hearts are abnormally primitive, advanced, or hypertrophied while still "preclinical", i.e., before the necrotizing, calcifying lesions of the cardiomyopathy appear. To do so we will continue our histological and electron microscopic quantitative analysis to accurately describe the difference in ventricular form or mass and in myocardial cell density or maturation, as they arise. Our second aim is to analyze the chronotopic and inotropic properties of these "preclinical" hearts, especially to explore their responses to calcium, to catecholamines, or to other agents which modify the availability of these substances to myocardial cells. We will do the studies on heart beating rate using cultured hearts, and those on contractility using papillary muscle strips connected to especially modified transducers. This study should help resolve the present controversy on the morphology of "preclinical" CM hearts and should help to fill large gaps in present knowledge of their physiology. It should contribute significantly to unravelling the factors which cause cardiomyopathy from those which aggravate the condition or simply result from it.